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Anna and louise > Vulva dermatoses > Flashcards

Vulva dermatoses Flashcards

1
Q

Blood supply to the female external genitalia

A

comes from the internal and external pudendal arteries
- Drains through corresponding veins

The external pudendal artery (branch of the femoral) has superficial and deep branches

Anterior division of the internal iliac artery –> internal pudendal artery

Within the pudendal canal

  • Inferior rectal artery
  • Perineal artery

Within the urogenital triangle

  • The artery of the vestibule
  • The deep artery of the clitoris
  • The dorsal artery of the clitoris
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2
Q

Lymphatic drainage of the vulva

A

Via the inguinal glands

Perineum and vulva have bilateral lymph drainage
- 1 side can drain to the unilateral and contralateral LN

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3
Q

Nerve innervation to the vulva

A

Pudendal nerve (S2-4)

  • Leaves the pelvis through the greater sciatic foramen and crosses the external surface of the ischial spines and re-enters the pelvis via the lesser sciatic notch, then splits into three
  • Inferior rectal (haemorrhoidal) nerve
  • Perineal nerve which branches into the posterior labial nerve
  • Dorsal nerve of the clitoris

Branches of the ilioinguinal nerve (L1)
Genital branch of the genitofemoral nerve (L1-2)
The perineal branch of the femoral cutaneous nerve of the thigh (L2-4)

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4
Q

Development of the vulva - physiology

A

Birth to puberty:
- Absence of glycogen –> lack of lactobacilli –> neutral / alkalinity –> increased chance of vulvovaginitis, UTI

Oestrogen –> thickening of vaginal epithelium + appearance of intracellular glycogen –> pH falls to 4-5

If pregnancy occurs, vulva can become congested with varicosities from increased progesterone and gravid uterus

Menopause - Significant fall in oestrogen, progesterone

  • Vagina becomes narrower, less rugose, drier
  • Amount of cellular glycogen reduces, epithelium becomes thinner
  • Vaginal pH becomes alkaline
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5
Q

LICHEN SCLEROSUS - aetiology

A

Auto-antibodies for extracellular matrix protein 1
Increased associated with other autoimmune diseases among patients (30% have autoimmune condition, 30% have family history)
- Thyroid disorders, alopecia areata, pernicious anaemia, T1DM, vitiligo - TEST TFTS / THYROID ABS

Higher incidence of disease in first degree relatives
- 10% FHx

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6
Q

LICHEN SCLEROSUS

- histology

A

Epidermal thinning (atrophic)
Hyperkeratosis
Wide band of collagen below the dermoepidermal junction
Lymphocytic infiltrate beneath this area

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7
Q

LICHEN SCLEROSUS

- clinical features

A

Two peak ages of presentation:

  • Prepubescent girls (~5% of all cases)
  • Post-menopausal women

Signs:
- Pale, white atrophic areas affecting the vulva
- Purpura (ecchymosis)
- Fissuring
- Erosions (but blistering is rare)
- Hyperkeratosis
- Localised or ‘figure of eight’ distribution
- Loss of architecture - loss of labia minora and/or midline fusion, burying of clitoral hood
- Extra genital lichen sclerosus in 1 in 10 (usually eyelids or back)
Does not involve the mucosa / vagina

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8
Q

LICHEN SCLEROSUS - treatment

A 
No definitive treatment / cure - chronic
Aim:
- Relieve symptoms 
- Normalise appearance (prevent further changes)
- Prevent scarring

Clobetasol proprionate 0.05%

  • Daily for 1/12, alternate days for 1/12, twice weekly for 1/12, then review at 3/12
  • Should have maintenance indefinitely

Good skin care
Emollients
Patient education is key

Follow up

  • <5% risk of SCC
  • once asymptomatic, yearly review
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9
Q

Lichen planus

- aetiology

A

Autoimmune inflammatory condition
Disorder of altered T-cell mediated immunity to exogenous antigens targeting the basal keratinocytes of the epidermis, genetic factors

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10
Q

Lichen planus

- clinical features

A

Usually post-menopausal (40-60y)
Typically presents with pain rather than pruritis
- Also vaginal discharge, sorenesss, burning, bleeding with sex
Erosion of mucosal surface of introitus, extending into vagina and involving cervix
Red, erythematous
- Lacy white lines (Wickham’s striae) in surrounding skin / on top
Vaginal lesions can lead to scarring and complete stenosis
Oral and genital lesions together in 70%

Three variants

  • erosive - most common
  • classical
  • hypertrophic
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11
Q

Lichen planus

- histology

A

Lymphocytic infiltrate in the upper dermis directed against the basement membrane zone
Irregular saw-toothed acanthosis

lack of basement membrane thickening or epidermal atrophy favour lichen planus over lichen sclerosus

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12
Q

Lichen planus

- treatment

A 
Limited evidence - treatment resistant
Topical steroids (clobetasol propionate)
Topical tacrolimus
Oral steroids, retinoids, immune suppression
refer specialist

Lifetime risk of invasive vulval cancer in the order of 2-4%

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13
Q

Contact dermatitis - irritant

Pathogenesis

A

Due to skin injury by prolonged pressure and irritation, chemical or physical agents –> inflammation
Reduces the integrity of the epidermis increasing the irritancy of irritants
Immediate, non-immunological, local inflammatory reaction
Can get secondary infection

More common (80%) than allergic contact dermatitis

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14
Q

Contact dermatitis - allergic

A

Caused by immune response following skin contact with an allergenic substance
Classical delayed-type hypersensitivity reaction (type IV, T cell mediated)

Identify allergen by patch teaching

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15
Q

Clinical features of contact dermatitis

A

Well demarcated margins in area of contact
Erythema, erosions, ulcers, tissue destruction
Increases with multiple exposure

Irritant - Rapid onset of Sx (mins to hrs)

Allergic - Delayed onset (1-2 days)
- may occur at distant site

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16
Q

Advice for contact irritant dermatitis

A

Avoid soaps, bubble baths, deodorants, feminine sprays, vaginal wipes
- Use non-perfumed emollient soap
Clean the vulval area with water only, showers > baths
If PU –> worse symptoms, wash urine away using warm water
Clean once a day only - Avoid scrubbing
Avoid creams that have not be prescribed
Avoid anti-septics in the bath
Wear loose-fitting cotton underwear
Use lubricants during sex
Use tampons over pads
Only apply creams and ointments where needed
- Ointments less likely to irritate and have fewer potential sensitisers

No G strings, jeans, lyra gym pants
No vaginal douching

17
Q

Histology of contact dermatitis

A

Variable features - key feature = spongiosis, irregular hyperkeratosis of epidermis
Allergic - more eosinophils
Contact - less eosinophils

18
Q

Treatment for contact dermatitis

A

If obese, weight reduction may help
Emollients - e.g. aqueous cream
Manage urinary incontinence
Topical corticosteroids with anti-bacterial / fungal

19
Q

VULVAL ECZEMA = ATOPIC DERMATITIS

A

Uncommon, even with widespread eczema
chronic inflammatory dermatosis characterised by relapsing episodes of flares of intensely pruritic, inflammatory skin lesions
Occasionally skin scaling and fissuring
Usually have eczema elsewhere

Spongiosis = intercellular oedema - characteristic of eczematous dermatitis

20
Q

LICHEN SIMPLEX CHRONICUS

- aetiology

A

Acquired severely itching chronic dermatosis characterised by a non-scarring process of epidermal thickening due to repeated scratching

Primary / idiopathic - on background of normal skin
Secondary - may be an underlying cause (e.g. lichen planus or lichen sclerosus)

21
Q

LICHEN SIMPLEX CHRONICUS

- clinical features

A

Long Hx of pruritis that hasn’t responded to any topical agent
May be worse at times of stress, at night
Asymmetry of the vulval lichenification with the clinically obvious side being the same side as the dominant hand
Mostly affects hair-bearing skin of labia majora

  • Skin thickening, erythematous lichenified plaques, leathery feeling skin
  • Skin excoriation, erosions, ulcers
22
Q

LICHEN SIMPLEX CHRONICUS

- histology

A

Hyperplasia of squamous epithelium, thickened epidermis, and hyperkeratosis – not atrophy / thinning as in lichen sclerosus
Spongiosis

23
Q

Lichen simplex chronics

- management

A

Treat underlying dermatoses / systemic disease
Remove triggers / exacerbating factors
Break the ‘itch-scratch cycle’
Topical corticosteroids (if lichenified areas)
Antihistamines at night to help sleep
Emollients
Repair barrier function of skin

24
Q

Define Hyperalgesia

A

exaggerated response to noxious substances through a general increase in the responsiveness of tissues

25
Q

Allodynia

A

production of pain by stimuli that does not usually cause pain by a reduction in the sensory threshold of the local neuronal pathways

26
Q

Vulvodynia - aetiology

and definition

A

Lifetime: 10-15%

Vulvodynia - vulvar pain of at least 3 months without clear identifiable cause, which may have potential associated factors
- diagnosis of exclusion

27
Q

Chronic pain pathophys

A

2 neurophysiological mechanisms implicated

Nociceptive

  • Injury to a pain sensitive structure
  • Somatic, visceral

Non-nociceptive
- Neuropathic
○ Pain as a result of changes in the nerve itself
○ Result of an insult to the CNS or PNS
○ Typical characteristics - burning pain, paraesthesia, lancinating pain
- Psychogenic

28
Q

Key history for vulvodynia

A

Unprovoked

  • Continuous sensation
  • Spontaneous pain
  • Itching not usually a problem

Provoked

  • Pain with light touch
  • Usually no symptoms at other times
  • May be multifactorial - Hx of vulvovaginal candidiasis is the most common feature

Localised, generalised
Aggravating and relieving factors
Psychosexual Hx
Co-morbidities and other pain syndromes (e.g. painful bladder syndrome, fibromyalgia, IBS, temporomandibular disorder)

29
Q

Treatment principles of vulvodynia

A

MDT - gynaecologist, physiotherapy, psychologist, pain specialist
The aim of therapy is to optimise pain control, enhance psychological and physical wellbeing and improve quality of life
The end points in the treatment include reducing the triggers of irritation, blocking peripheral nociceptors, central inhibition, tackling pelvic floor dysfunction and addressing psychosexual dysfunction

The “4 Ps”

  • Patient education and reassurance
  • Pain modification
  • Physical therapy
  • Psychological and psychosexual therapy
30
Q

Treatment of provoked vulvodynia

A 
Avoid irritants
Emollient soap substitute
Topical LA (2 or 5%) - use with caution 
Pelvic floor muscle biofeedback
Vaginal TENS
Vaginal dilators 
Vestibulectomy
- Surgical removal of hyperaesthetic skin
- If responded to topical lidocaine prior to sex, more likely to have a better outcome
- Complete response rate 59%
31
Q

Genital warts - aetiology

A

90% caused by HPV 6 or 11

Transmission

  • Sexual contact - Condoms reduce but do not eliminate risk
  • Perinatal

Average incubation period 3 months
90% reduction in cases (15-20y) since Gardasil introduced

32
Q

Treatment options for genital warts

A

Is largely cosmetic
30% have spontaneous clearance over a 6 month period
No evidence Rx reduces risk of transmission

Imiquimod cream 5%

  • Topical, patient applied
  • Can weaken latex condoms, local skin irritation

Podophyllotoxin solution

  • Avoid in pregnancy
  • Patient applied

Cryotherapy - Freezing therapy
- can do in pregnancy

Diathermy, laser, excision

  • Single treatment
  • Can distort anatomy
  • may need GA
33
Q

Genital warts in pregnancy

A

Common for warts to occur / recur during pregnancy
More likely to be symptomatic
- Anogenital warts can be extensive and rapidly enlarging
- Likely consequence of altered immunity and increased blood supply

Vertical transmission of HPV occurs in up to 1 in 80
- Can cause genital and laryngeal warts in infants

CS can be consider if large warts that may obstruct labour or that cause extensive cervical disease
Otherwise not indicated

34
Q

Expectant vs. active treatment for warts

A

The treatment of genital warts is largely cosmetic
They can spontaneously regress in 30% people over the course of 6 months
No evidence that treating warts lowers risk of passing on HPV
Reassure low oncogenic potential

Active treatment can be indicated:
- If the patient requests it
- If they are symptomatic or causing irritation
Recurrence of 30% regardless of treatment
Psychological impact

Anna and louise (28 decks)

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